Lacking evidence for calcium-binding protein fetuin-A to be linked with chronic kidney disease-related pruritus (CKD-rP).

Sir,

Uraemic pruritus, now better known as chronic kidney disease-related pruritus (CKD-rP), is still a commonly experienced, tormenting and challenging symptom in patients with chronic kidney diseases [1].

There has been an ongoing discussion whether pruritus in chronic kidney disease is brought about by the common disturbance of calcium/phosphate homeostasis [2].

Recently it has been proposed that a vicious circle of metabolic derangements (malnourishment, inflammation, arteriosclerosis) may explain the exaggerated morbidity and mortality in a subset of haemodialysis patients [3]. Inflammation might be the most deleterious factor in this respect which, besides other factors, is related to the occurrence of CKD-rP and down-regulation of fetuin-A, an important calcium-binding circulating protein favouring tissue-calcifications in these patients [4].

Thus, we were interested in whether patients with CKD-rP display lower levels of serum fetuin-A.

Ten patients in a hospital-based haemodialysis centre complaining about CKD-rP were compared to another 12 patients who did not report to have suffered from CKD-rP at least 6 months prior to the interview. Patients with CKD-rP were asked to score the intensity of current pruritus using a visual analogue scale (VAS) ranging from 0 to 10. In both groups, 10 ml of blood was taken immediately after puncture of the arterio-venous fistula, and fetuin-A, 25-hydroxyvitamin D3 (25[OH]D3), total protein, albumin, calcium (corrected for serum albumin), phosphate, and high-sensitivity CRP (hsCRP) were measured.

Independent t-tests (continuous variables) and a χ2-test (gender) evaluated whether there were significant (P < 0.05) differences between patients with and without CKD-rP.

The mean pruritus intensity of patients with CKD-rP was 5.9 ± 1.9. After identifying one univariate outlier (hsCKP = 35.6) in the group of patients without CKD-rP, CRP was significantly higher in patients with CKD-rP. We failed, however, to find significant differences in serum-calcium, phosphate, fetuin A and 25-OH-Vitamin D3 between the two groups (Table 1). Additionally, there was no relationship between the intensity of CKD-rP and the metabolic factors measured (including CRP) in patients suffering from pruritus.

Table 1

Patient and clinical characteristics between the two groups. PTH (intact parathyreoid hormone), hsCRP (high-sensitivity C-reactive protein), 25(OH)D3 (25-hydroxyvitamin D3)

	CKD-rP	No CKD-rP
	n = 10 M (SD)	n = 11 M (SD)	P
Kt/V	1.5 (0.40)	1.3 (0.28)	0.28
Age	66.2 (12.7)	66.5 (13.9)	0.48
Male [n (%)]	5 (50.0)	8 (72.7)	0.39
Female [n (%)]	5 (50.0)	3 (27.3)
Time on haemodialysis
in months	40.6 (30.5)	38.7 (50.1)	0.92
Current use of
1-OH-vitamin D	0.5 (0.5)	0.7 (0.5)	0.31
Current use of cinacalcet	0.3 (0.5)	0.5 (0.5)	0.28
PTH (ng/L)	317.5 (334.0)	525.8 (474.3)	0.26
Fetuin A (g/L)	0.4 (0.1)	0.4 (0.1)	0.53
Corrected calcium	2.3 (0.2)	2.2 (0.2)	0.45
Calcium (mmol/L)	2.2 (0.2)	2.2 (0.2)	0.48
Protein (g/L)	69.3 (4.7)	68.4 (4.5)	0.65
Albumin (g/L)	35.7 (3.3)	35.7 (5.9)	0.99
HsCRP (mg/L)	12.5 (9.8)	4.1 (3.0)	0.02
25(OH)D3 (μg/L)	13.9 (4.0)	14.2 (6.3)	0.91
Phosphate (mmol/L)	1.8 (0.6)	1.8 (0.4)	0.73

Although our study approach has methodological limitations (small number of patients, no matched pairs) the results suggest that neither calcium-binding protein fetuin-A levels nor 25(OH)D3 values were noticeably different in patients with CKD-rP compared to patients without CKD-rP. On the other hand, the marker for inflammation, CRP, was found to be significantly higher in patients with CKD-rP as shown before [5]. We hence believe that other inflammation-driven processes need to be studied in the future in order to understand the pathomechanisms of CKD-rP.

Conflict of interest statement. None declared.